Programmed ventricular stimulation at a second right ventricular site: An analysis of 100 patients, with special reference to sensitivity, specificity and characteristics of patients with induced ventricular tachycardia

One hundred patients without ventricular tachycardia (VT) initiated from the right ventricular (RV) apex were subjected to stimulation at the RV outflow tract. Sixty-two patients had no clinical arrhythmias, and 38 had sustained VT, ventricular fibrillation (VF) or cardiac arrest. Of the 38 patients with clinical arrhythmias, 22 (58%) had VT or VF induced from the RV outflow tract. Among the 62 patients without arrhythmias, 5 (13%) had polymorphic nonsustained VT or VF induced, which occurred with triple extrastimull in all 5 patients. The 22 patients with VT initiated at the RV outflow tract were a heterogeneous group; 10 (45%) patients had cardiac diagnoses other than coronary artery disease (CAD). In contrast were patients whose VT was initiated at the RV apex (n = 84); in this group, 20 patients (22%) had diagnoses other than CAD (p <0.05). These 22 patients also were younger (mean age 46 years) than patients whose VT was initiated at the RV apex (mean age 58; p <0.01). Of the 16 patients with clinical VT and no induced arrhythmia from either RV site, 7 had CAD (4 with cardiac arrest), 5 had the long QT syndrome, 3 had dilated cardiomyopathy and 1 had valvular heart disease. In conclusion, stimuiation at a second RV site increases the sensitivity of RV stimulation in patients with known VT and seldom initiates VT in patients without cllnical VT.     

Spatial dispersion of action potential duration restitution kinetics is associated with induction of ventricular tachycardia/fibrillation in humans

INTRODUCTION: Action potential duration restitution (APDR) plays a role in initiation and maintenance of ventricular tachycardia (VT)/ventricular fibrillation (VF). We hypothesized that the steeply sloped APDR and its spatial heterogeneity contribute to VT/VF inducibility in patients with ventricular arrhythmia. METHOD AND RESULTS: After programmed ventricular stimulation (PVS) for evaluation of clinically documented VT, patients (n = 20, 15 male, age 52.5 +/- 9.5 years) were divided into two groups: inducible sustained VT/VF (IVT, n = 10) and noninducible VT/VF (NVT, n = 10). Data were compared with the corresponding results obtained from normal controls (C, n = 10). Right ventricular (RV) monophasic action potential duration at 90% repolarization (APD90) and ventricular effective refractory period (VERP) in the right ventricular apex (RVA) and right ventricular outflow tract (RVOT) were determined. APDR was acquired by scanning diastole with premature ventricular beats during a pacing cycle length of 600 msec (S1-S2) in all patients and by rapid pacing at the cycle lengths that induced APD alternans in three patients. Maximal slopes (Smax) of the APDR curves and DeltaAPD90 (APD90 at S2 400 ms - APD90 at the shortest S2) were measured. VERP and APD90 at each RV site did not differ among the three groups. Smax obtained by S1-S2 (1.6 +/- 0.6) did not differ from Smax obtained by rapid pacing (1.2 +/- 0.7), with a significant correlation noted between these values (r = 0.92, P < 0.01). The IVT group had a higher spatial dispersion of Smax (Smax at RVOT - Smax at RVA) compared to the C group (P < 0.05), with no difference between the NVT group and the IVT or C groups. The IVT group had a higher spatial dispersion of DeltaAPD90 compared to the NVT and C groups (P < 0.01, respectively). Smax at the RVOT (2.7 +/- 1.9) was steeper than that at the RVA (1.9 +/- 1.2, P < 0.05). Inducibility of sustained VT/VF was greater at the RVOT (83.3%) than at the RVA (50.0%, P < 0.05). CONCLUSION: In patients with ventricular arrhythmia, VT/VF is highly inducible under conditions of greater spatial dispersion of ventricular refractoriness and APDR.     

Frequency and significance of induced sustained ventricular tachycardia or fibrillation two weeks after acute myocardial infarction

Electrophysiologic study, 24-hour ambulatory electrocardiographic monitoring, treadmill exercise test and angiographic evaluations were performed in 45 patients 14 +/- 3 days (mean +/- standard deviation) after acute myocardial infarction. Electrophysiologic study protocol included burst ventricular pacing and 1 to 3 ventricular extrastimuli at 2 cycle lengths from right ventricular apex, right ventricular outflow and left ventricle. Sustained monomorphic ventricular tachycardia (VT) (13 patients) or ventricular fibrillation (VF) (7 patients) was induced in 20 patients (44%) (group I). In these 20 patients, VT/VF was inducible with 2 extrastimuli in 10 patients, 3 extrastimuli in 9 patients and burst pacing in 1 patient. In the remaining 25 patients (56%), induction of no fewer than 7 ventricular beats were noted (group II). Severe left ventricular (LV) wall motion abnormalities occurred in 70% of group I patients and 22% of group II patients (p less than 0.005). There was no difference in the site of infarction, frequency and grade of ventricular ectopic rhythm on ambulatory electrocardiographic monitoring, double product on submaximal exercise, LV ejection fraction, and number of obstructed coronary arteries (70% or greater) (p greater than 0.1) between group I and group II patients. During a mean follow-up of 10 +/- 3 months, 1 patient in each group died suddenly, and in 1 group I patient spontaneous sustained VT developed which was identical in morphologic configuration to that induced during electrophysiologic study. In conclusion, electrical induction of sustained VT or VF during electrophysiologic study is common in patients 2 weeks after acute myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)     

The clinical implications of cumulative right ventricular pacing in the multicenter automatic defibrillator trial II

INTRODUCTION: This study was designed to assess whether right ventricular pacing in the implantable cardioverter defibrillator (ICD) arm of the Multicenter Automatic Defibrillator Implantation Trial (MADIT) II was associated with an unfavorable outcome. METHODS AND RESULTS: Data on the number of ventricular paced beats were available in 567 (76%) of 742 MADIT II patients with ICDs. The number of ventricular paced beats over the total number of beats showed a bimodal distribution with patients being predominantly paced or nonpaced. Therefore, patients were dichotomized at 0-50% and 51-100% of cumulative pacing with median pacing rate 0.2% and 95.6%, respectively. Endpoints included new or worsening heart failure, appropriate ICD therapy for VT/VF, and the combined endpoint of heart failure or death. Clinical features associated with frequent ventricular pacing included age >or=65 years, advanced NYHA heart failure class, LVEF < 0.25, first degree AV and bundle branch block, and amiodarone use. During follow-up, 119 patients (21%) had new or worsened heart failure, 130 (23%) had new or worsened heart failure or death, and 142 (25%) had appropriate therapy for VT/VF. In comparison to patients with infrequent pacing, those with frequent pacing had significantly higher risk of new or worsened heart failure (hazard ratio = 1.93; P = 0.002) and VT/VF requiring ICD therapy (HR = 1.50; P = 0.02). CONCLUSIONS: Patients in MADIT II who were predominantly paced had a higher rate of new or worsened heart failure and were more likely to receive therapy for VT/VF. These results suggest the deleterious consequences of RV pacing, particularly in the setting of severe LV dysfunction.     

Acute blood pressure effects at the onset of supraventricular and ventricular tachycardia

This study was designed to assess the effects of tachycardia origin, the significance of atrial contribution, and the effects of left ventricular ejection fraction on hemodynamically tolerated ventricular tachycardia (VT) and supraventricular tachycardia (SVT). Forty-one subjects with inducible hemodynamically tolerated VT (n = 24) or SVT (n = 17) with mean ages of 60 ± 13 and 40 ± 16 years and mean ejection fractions of 32 ± 15% and 59 ± 5%, respectively, were studied. VT and SVT were induced by standard techniques, and femoral arterial blood pressure (BP) was recorded for 30 seconds. After tachycardia termination, with ≥3 minutes between conditions, ventricular overdrive pacing was performed from the right ventricular (RV) apex and then the RV outflow tract, followed by atrioventricular (AV) pacing at the tachycardia cycle length. Mean BP was measured every 5 seconds. Linear regression methods were used to model BP response for the 2 groups. There was a significant increase in BP over the 20-second interval after the induction of VT and SVT (0.55 ± 0.21 and 1.0 ± 0.20 mm Hg/s, respectively, p <0.05). In patients with hemodynamically tolerated VT, RV apex and RV outflow tract pacing at the tachycardia cycle length decreased BP by 6.7 ± 2.0 (p <0.002) and 4.7 ± 2.5 mm Hg (p = 0.06), respectively. AV pacing at the tachycardia cycle length did not improve BP compared with RV pacing alone. In patients with SVT, RV apex and RV outflow pacing at the tachycardia cycle length decreased BP by 5.6 ± 2.9 (p = 0.05) and 4.1 ± 2.7 mm Hg (p = 0.12), respectively. However, AV pacing at the tachycardia cycle length was associated with improved BP response over RV pacing alone. Increased age and lower ejection fraction adversely influenced BP response in the VT group and longer cycle length, and higher preinduction BP favorably influenced BP response in the SVT group. The determinants of BP response after tachycardia onset are complex and differ in patients with SVT and VT.     

Programmed electrical stimulation in healed myocardial infarction using a standardized ventricular stimulation protocol

The diagnostic accuracy of programmed electrical stimulation was prospectively assessed in 111 patients with myocardial infarction (MI) with or without a history of spontaneous ventricular arrhythmias. In 29 patients neither ventricular tachycardia (VT) nor episodes of 10 premature ventricular depolarizations per hour was documented. Fifty patients had documented nonsustained VT and 32 had sustained monomorphic VT. One and 2 extrastimuli (twice diastolic threshold, 2 ms in duration) were given during sinus rhythm and ventricular pacing at 100, 120 and 140 beats/min in the right ventricular apex (part I). When this protocol failed to induce a sustained monomorphic VT, a third extrastimulus was introduced (part II). Repetitive ventricular responses were induced in all patients, and in 15 (14%) polymorphic ventricular arrhythmias requiring DC shock were induced. Incidence of initiation of sustained monomorphic VT and polymorphic ventricular arrhythmias requiring DC shock was related to the clinical arrhythmia and the stimulation protocol. In patients with documented sustained monomorphic VT, a third extrastimulus only increased the incidence of sustained monomorphic VT (68% to 94%), whereas in patients with documented nonsustained VT and without VT the incidence of both polymorphic and monomorphic arrhythmias increased by 7 to 12%. Sustained monomorphic VTs induced in patients without such a history were faster (p less than 0.01), depended on site of MI (p less than 0.05) and were more often preceded by nonsustained polymorphic VT (p less than 0.01) than in patients with documented sustained monomorphic VT.(ABSTRACT TRUNCATED AT 250 WORDS)     

Discordant results of programmed ventricular stimulation at different right ventricular sites in patients with and without spontaneous sustained ventricular tachycardia: a prospective study of 56 patients

Programmed ventricular stimulation (PVS) was prospectively performed in 56 consecutive patients from both the right ventricular (RV) apex and the RV outflow tract. Thirty-seven patients had documented clinical sustained ventricular tachycardia (VT) and 19 patients had no sustained spontaneous VT in the absence of antiarrhythmic drugs. The sensitivity of VT induction was 65% from the RV apex, 76% from the RV outflow tract and was 89% with combined stimulation at both RV sites. The specificity from the RV apex, the RV outflow tract and both sites combined was 100%. When sustained VT was induced from both sites (51%), it was usually of the same morphologic characteristics, axis and cycle length. When sustained VT was induced at 1 site and nonsustained VT at the second site, the morphologic characteristics or axis usually differed. Of patients who had VT induced at both RV sites during the baseline study 37% had VT rendered noninducible during treatment with conventional antiarrhythmic agents. No patients whose VT was induced at only 1 RV site responded to conventional drugs. We conclude that programmed ventricular stimulation at a second RV site is frequently helpful in the evaluation of VT. Inducibility at only 1 of 2 RV sites predicts a poor response to conventional antiarrhythmic drugs.     

Complex ventricular ectopic activity in patients less than 20 years of age with or without syncope, and the role of ventricular extrastimulus testing

To assess the potential for ventricular tachycardia (VT), ventricular extrastimulus testing was performed in 33 young patients with complex ventricular ectopic activity defined as multiform ventricular premature complexes (VPCs), couplets or nonsustained VT, or a combination, found during electrocardiographic monitoring. There were 21 male and 12 female patients with a mean age of 11 years (range 1 to 18). Patients were divided into 2 groups based on the presence (14 patients) or absence (19 patients) of syncope. Patients with syncope had ostensibly normal hearts (9 patients) or miscellaneous heart disease (5 patients). Patients without syncope had ostensibly normal hearts (8 patients) or miscellaneous heart disease (11 patients). Ventricular stimulation protocol consisted of burst pacing and 1 to 4 programmed extrastimuli decreasing to refractoriness at 3 drive-train cycle lengths, and at 2 pacing sites (right ventricular apex and outflow tract) during the drug-free baseline state and isoproterenol infusion. No patient had VT induced with 1 or 2 extrastimuli. VT was induced in 13 of 14 patients (93%) with syncope, and in 9 of 19 patients (47%) without syncope (p less than 0.05). Using a 3-extrastimuli protocol, 8 of 14 patients (57%) with and 3 of 19 patients (16%) without syncope had VT induced (p less than 0.05). These findings suggest that VT may be the cause of syncope in young patients with complex ventricular ectopic activity.     

Prospective comparison of right and left ventricular stimulation for induction of sustained ventricular tachycardia

Thirty-eight patients who had sustained monomorphic ventricular tachycardia (VT) or sudden cardiac death underwent programmed ventricular stimulation. To assess the relative efficacy of right and left ventricular (RV and LV) stimulation, a tandem protocol with 1 to 4 extrastimuli and burst pacing was used. Each step of the protocol was performed in a rotating sequence at the RV apex, basal RV septum and LV apex. Sustained VT was induced from the RV apex in 26 patients, right ventricle (either site) in 27, and LV apex in 24, and spontaneous VT was reproduced from those sites in 11, 14 and 12 patients, respectively. In the 23 patients who had sustained VT induced from both ventricles, RV stimulation always required fewer or the same number of extrastimuli for induction. At every stage of the protocol, the cumulative yield of sustained VT was consistently greater from the right ventricle than from the left ventricle. After delivering 4 extrastimuli and burst pacing, LV stimulation only increased the yield of sustained VT by 1 patient, and spontaneous VT by 3 patients. Inducibility or noninducibility in the right ventricle generally predicted the same outcome in the left ventricle. Previously undocumented VT or ventricular fibrillation was induced from the right ventricle in 19 patients and from the left ventricle in 13. Thus, LV stimulation was less efficacious than RV stimulation. LV stimulation increased the yield over RV stimulation only minimally and did not reduce the number of extrastimuli required to induce sustained VT.     

Right ventricular pacing is an independent predictor for ventricular tachycardia/ventricular fibrillation occurrence and heart failure events in patients with an implantable cardioverter-defibrillator

Aims: There is increasing evidence that right ventricular (RV) pacingmay have detrimental effects by increasing morbidity and mortalityfor heart failure in implantable cardioverter–defibrillator(ICD) patients. In this study we prospectively tested the hypothesisthat cumulative RV pacing increases ventricular tachycardia/ventricularfibrillation (VT/VF) occurrence (primary endpoint) and hospitalizationand mortality for heart failure (secondary endpoint) in a predominantlysecondary prophylactic ICD patient population. Methods and results: Two hundred and fifty patients were divided into two groupsaccording to the median of cumulative RV pacing (2 vs. >2%)and prospectively followed-up for occurrence of primary andsecondary endpoints for 18 ± 4 months. Established predictorsfor VT/VF occurrence and heart failure events such as age, leftventricular ejection fraction (EF), QRS duration, history ofatrial fibrillation, and NT-proBNP were collected at enrolment.Multivariate Cox regression analysis revealed that cumulativeRV pacing > 2% and EF < 40% were independent predictorsfor VT/VF occurrence and heart failure events. Kaplan–Meieranalysis showed that patients with >2% cumulative RV pacingmore frequently suffered from VT/VF occurrence and heart failurehospitalization. Conclusion: Cumulative RV pacing > 2% and EF < 40% are independentpredictors for VT/VF occurrence and mortality and hospitalizationfor heart failure in predominantly secondary prophylactic ICDpatients. Our data show that algorithms capable of reducingcumulative RV pacing should be used more frequently in clinicalpractice.     

Electrocardiographic characteristics of repetitive monomorphic right ventricular tachycardia originating near the His-bundle

INTRODUCTION: Most idiopathic nonreentrant ventricular tachycardia (VT) and ventricular premature contractions (VPCs) arise from the right or left ventricular outflow tract (OT). However, some right ventricular (RV) VT/VPCs originate near the His-bundle region. The aim of this study was to investigate ECG characteristics of VT/VPCs originating near the His-bundle in comparison with right ventricular outflow tract (RVOT)-VT/VPCs. METHODS AND RESULTS: Ninety RV-VT/VPC patients underwent catheter mapping and radiofrequency ablation. ECG variables were compared between VT/VPCs originating from the RVOT and near the His-bundle. Ten patients had foci near the His-bundle (HIS group), with the His-bundle local ventricular electrogram preceding the QRS onset by 15-35 msec (mean: 22 msec) and His-bundle pacing produced a nearly identical ECG to clinical VT/VPCs. The HIS group R wave amplitude in the inferior leads (lead III: 1.0 +/- 0.6 mV) was significantly lower than that of the RVOT group (1.7 +/- 0.4 mV, P < 0.05). An R wave in aVL was present in 6 of 10 HIS group patients, while almost all RVOT group patients had a QS pattern in aVL. Lead I in HIS group exhibited significantly taller R wave amplitudes than RVOT group. HIS group QRS duration in the inferior leads was shorter than that of the RVOT group. Eight of 10 HIS group patients exhibited a QS pattern in lead V1 compared to 14 of 81 RVOT group patients. HIS group had larger R wave amplitudes in leads V5 and V6 than RVOT group. CONCLUSION: VT/VPCs originating near the His-bundle have distinctive ECG characteristics. Knowledge of the characteristic QRS morphology may facilitate catheter mapping and successful ablation.     

Programmed ventricular stimulation using up to two extrastimuli and repetition of double extrastimulation for induction of ventricular tachycardia: a new highly sensitive and specific protocol

The sensitivity and specificity of a new protocol of programmed ventricular stimulation were evaluated in 71 consecutive patients who were divided into 2 groups: group 1 included 41 patients, of whom 25 had sustained ventricular tachycardia (VT) not associated with cardiac arrest and 16 had ventricular fibrillation (VF) not precipitated by any obvious factor; group 2 included 30 patients without demonstrable heart disease and no suspected or documented sustained ventricular tachyarrhythmias. The study consisted of a standard protocol (up to 2 extrastimuli given only once for each extrastimulus prematurity, 2 right ventricular sites and 3 basic pacing cycle lengths, as well as rapid ventricular pacing) in which double extrastimulation at the shortest coupling intervals that allowed ventricular capture was repeated 10 times. A stimulus current of 3 mA was used. Sustained ventricular tachyarrhythmias were induced in 23 of 25 (92%) patients who presented with sustained VT, 14 of 16 (88%) patients who presented with VF and 2 of 30 (7%) group 2 patients. Eighteen of 25 (72%) patients with sustained VT but only 4 of 16 (25%) with VF had arrhythmias inducible at "immediate" trials of single or double extrastimulation (p less than 0.01). Repetition of double extrastimulation increased the yield of inducible sustained ventricular tachyarrhythmia to 92% in patients with sustained VT (+20%, p = 0.14) and 75% (+50%, p = 0.013) in patients with VF. Rapid right ventricular pacing added a 13% increase in the overall yield in patients with VF. This new protocol of programmed ventricular stimulation has both high sensitivity (90%) and specificity (93%) for induction of sustained VT.(ABSTRACT TRUNCATED AT 250 WORDS)     

Successful catheter ablation in a patient with polymorphic ventricular tachycardia

We describe a patient with polymorphic ventricular tachycardia (PVT)/ventricular fibrillation (VF) without organic heart disease who was cured by radiofrequency catheter ablation. The patient was a 65-year-old woman with a 10-year history of recurrent syncope. There was no evidence of organic heart disease, and the QT interval during sinus rhythm was borderline normal (corrected QT interval = 0.45 sec1/2). ECG recording during syncope showed PVT. On one occasion, PVT degenerated into VF. This PVT was always induced by a premature ventricular complex (PVC) originating from the right ventricular (RV) outflow tract. Rapid pacing (220 beats/min) at the site of PVC origin reproduced polymorphic change of the QRS wave on surface ECG that was similar to PVT. This suggests that the PVT originated from a single focus in the RV outflow tract. Catheter ablation was performed at the site of PVC origin. During 18-month follow-up, PVT/VF was not documented.     

Ventricular late potentials and induced ventricular arrhythmias after surgical repair of tetralogy of Fallot.

Ventricular tachycardia (VT) and sudden death are rare but recognized complications after surgical repair of tetralogy of Fallot. We prospectively studied 31 patients (19 boys and 12 girls, mean age +/- standard deviation 7 +/- 4 years) with postoperative tetralogy of Fallot, by means of right-sided cardiac catheterization, 24-hour Holter monitoring, body-surface and intracavitary signal-averaging (gain 10(5) to 10(6), filters of 100 and 300 Hz) and programmed ventricular stimulation (1 and 2 extrastimuli, 3 basic cycle lengths, right ventricular apex and outflow tract). All patients were asymptomatic and none had documented or suspected ventricular arrhythmias. Ventricular late potentials were detected in 10 of 31 patients (32%) and spontaneous ventricular arrhythmias in 12 of 31 patients (39%). No sustained VT was induced by programmed ventricular stimulation but nonsustained VT was induced in 3 patients (10%). Patients with inducible VT more often had late potentials (3 of 3 vs 7 of 28, p less than 0.01), and spontaneous ventricular premature complexes (VPCs) during Holter monitoring (3 of 3 vs 9 of 28, p less than 0.05). To predict VT inducibility, late potentials had a sensitivity of 100%, a specificity of 75%, a positive predictive value of 30% and a negative predictive value of 100%. For spontaneous VPCs, the figures were 100, 68, 25 and 100%, respectively. It is concluded that shortly after repair of tetralogy of Fallot, the presence of both spontaneous VPCs and ventricular late potentials are associated with an increased incidence of inducible VT. Conversely, the absence of VPCs and ventricular late potentials may identify patients at low risk of subsequent ventricular arrhythmias.     

Identifying patients at risk of sudden death after myocardial infarction: Value of the response to programmed stimulation, degree of ventricular ectopic activity and severity of left ventricular dysfunction

The ability of programmed ventricular stimulation to identify risk of sudden death after acute myocardial infarction (MI) was compared with 24-hour electrocardiographic assessment of ventricular ectopic activity and determination of left ventricular (LV) dysfunction. Forty-six patients underwent programmed stimulation 8 to 60 days (mean 22) after documented MI. Programmed stimulation consisted of single and double extrastimuli from the right ventricular apex at 2 times diastolic threshold during ventricular pacing and normal sinus rhythm. Of the 46 patients, 44 underwent electrocardiographic monitoring at least 6 days after MI. In 43 of the 46 patients, LV ejection fraction (EF) and the presence of LV aneurysm were determined. In response to programmed ventricular stimulation, 5 patients had sustained ventricular tachycardia (VT), 5 had nonsustained VT (≥4 beats), 13 had intraventricular reentrant repetitive responses, and 23 had either bundle branch reentrant repetitive responses or no extra responses to programmed ventricular stimulation (negative study).

During a mean follow-up of 18 months, 10 patients died, 6 suddenly. One of the 10 patients with sustained or nonsustained VT died suddenly, compared with 3 of 13 patients with intraventricular reentrant responses and 2 of 23 patients with a negative study (difference not significant). Of 25 patients with Grade 0 to 2 ventricular ectopic activity, 3 died suddenly after MI, compared with 3 of 19 patients with Grade 3 or 4 activity (difference not significant). By comparison, the frequency of sudden death was greater in patients with an LVEF of <40% (5 of 16 versus 1 of 27 patients) or an LV aneurysm (5 of 13 versus 1 of 30 patients).

Thus, using the described protocol, the response to programmed ventricular stimulation is not helpful in identifying patients at risk for sudden death after MI. The presence of an LV aneurysm or EF of <40% appears to provide the greatest prognostic information with respect to risk for sudden cardiac death.     

Acute effects of His bundle pacing versus left ventricular and right ventricular pacing on left ventricular function

Dual-chamber pacing with His bundle pacing has theoretical advantages over conventional right ventricular (RV) apical pacing. We compared indexes of left ventricular (LV) function during acute dual-chamber pacing from the His bundle and other RV and LV pacing sites. Twelve patients (6 men; 63 +/- 11 years) with a standard indication for electrophysiologic study were included. Average QRS duration was 100 +/- 19 ms. Ejection fraction was 48 +/- 15%. A pressure-volume catheter was positioned in the left ventricle through the femoral arterial access. Pressure-volume loops were collected during atrial (AAI) and dual-chamber overdrive pacing at 82 +/- 15 beats/min after 2 minutes of hemodynamic stabilization. Ventricular pacing catheter position was randomized between the RV apex, RV septal, and free wall portions of the outflow tract, LV free wall, and His bundle. His bundle capture was verified from surface electrocardiographic morphometry using standard criteria. Atrioventricular delay was set to the P wave-His duration -10 ms to minimize the effects of fusion (96 +/- 22 ms). LV only pacing, but not His pacing, resulted in improved stroke work and stroke volume compared with alternate site RV pacing. No changes in +dP/dt, LV end-systolic pressure. LV end-diastolic pressure, or cycle efficiency, were observed between RV pacing sites. In conclusion, acute His bundle pacing did not improve LV function compared with alternate site RV pacing and may be inferior to LV pacing.     

Programmed ventricular stimulation in mitral valve prolapse: analysis of 36 patients

Programmed ventricular stimulation with 3 extrastimuli was performed in 36 patients with mitral valve prolapse (MVP). Among 11 patients without transient cerebral symptoms, none had inducible ventricular tachycardia (VT) or ventricular fibrillation (VF), whether or not nonsustained VT or ventricular premature complexes (VPC) were present during ambulatory electrocardiographic recordings. These patients remained well without antiarrhythmic drug therapy for 6 to 57 months (mean 23) of follow-up. Two patients with recurrent unexplained syncope and no documented ventricular arrhythmia during electrocardiographic monitoring also had no inducible VT or VF. Among 20 patients with syncope or presyncope and documented nonsustained VT or VPCs during electrocardiographic monitoring, polymorphic nonsustained VT was induced in 8, sustained unimorphic VT in 2, and VF in 3. In 1 patient who had inducible polymorphic nonsustained VT, electrocardiographic monitoring during syncope showed sinus rhythm. Among 3 patients with a history of sustained VT or VF, unimorphic VT was induced in each. Patients with MVP who have asymptomatic ventricular ectopic activity and no inducible VT may have a benign prognosis without treatment. In patients who have transient cerebral symptoms and documented nonsustained VT or VPCs, VT or VF is inducible in 65%, most often polymorphic VT. It is unclear in which patients this finding is clinically significant and in which it is a nonspecific response to programmed stimulation.     

Limited value of programmed electrical stimulation from multiple right ventricular pacing sites in clinically sustained ventricular fibrillation or ventricular tachycardia associated with coronary artery disease

One-hundred and fifty patients with coronary artery disease and a documented history of sustained ventricular tachyarrhythmias were studied to determine if programmed electrical stimulation (PES) from a second right ventricular (RV) pacing site optimizes the induction of such sustained arrhythmias. The first PES test was performed from 2 RV pacing sites (apex and outflow tract or septum) using the apex first in each patient. All patients underwent a second PES within 6 to 24 hours of the first; both studies used up to 4 ventricular extrastimuli, in the absence of antiarrhythmic treatment. The second PES was performed from a single RV apical site using a pacing catheter retained from the first study. During the first day's study, 74 patients (49%) had sustained ventricular tachycardia induced from the RV apex. Only 11 of the remaining 76 patients (7% of the total group) were inducible exclusively from a second RV pacing location during the first day's testing. Seven of these 11 patients, as well as 15 additional patients who did not have ventricular tachycardia induced from either site on the first day's study, were inducible from the RV apex during the second drug-free study. Among patients with sustained ventricular tachyarrhythmias, limiting PES to a single RV site, with the option of performing a second study in those who are initially noninducible is more effective in inducing sustained ventricular tachyarrhythmias than is PES performed from 2 RV pacing sites.     

Tachycardia and ventricular fibrillation in the arrhythmogenic right ventricle (arrhythmogenic dysplasia of the right ventricle). Clinical and electrocardiographic spectrum

In this paper we report the arrhythmias recorded on basal ECG, on Holter monitoring or on exercise test, in 32 pts affected by arrhythmogenic right ventricle (ARV). A sustained ventricular tachycardia (VT) was present in 11 pts a non sustained VT in 15 pts, a slow VT in 2 pts, a ventricular fibrillation (VF) in 3 pts and both sustained VT and VF in 1 pt. All but 1 case of sustained VT showed a LBBB like pattern. The heart rate during VT ranged between 170 and 280 beats/min. The frontal axis of the VT showed a wide range of deviation. Among non sustained VT, 9 cases had LBBB like pattern and 6 cases had polymorphic configuration. The 2 cases of slow VT showed LBBB like pattern with right axis deviation. A comparison between ventricular arrhythmias and RV impairment was made. The data obtained suggest that the effort plays an important role in the induction of VT in pts with localized RV impairment. In conclusion a wide spectrum of ventricular tachyarrhythmias is present in the ARV. Probably the RV "arrhythmogenic" zones and the electrophysiological mechanism causing the arrhythmias are various.     

Hemodynamic benefits of synchronized 1:1 atrial pacing during sustained ventricular tachycardia with severely depressed ventricular function in coronary heart disease

The hemodynamic effects of atrial pacing were studied in 8 patients who had ventricular tachycardia (VT) during electrophysiologic testing. These patients had chronic recurrent VT associated with organic heart disease and depression of left ventricular function (ejection fraction = 0.23 to 0.35). Hemodynamic variables were recorded during sinus rhythm (58 to 103 beats/min), pacing-induced VT (133 to 214 beats/min) and synchronized 1:1 triggered atrial pacing (atrium paced, ventricle sensed and triggered mode) during VT. For the latter, the ventriculoatrial coupling interval was adjusted to produce a maximal blood pressure response; the optimal interval was observed to be between 60% and 73% of the RR interval. Mean arterial blood pressure decreased after the onset of VT (90 +/- 11 to 79 +/- 14 mm Hg, p less than 0.05) but increased again when atrial pacing was added, to 98 +/- 12 mm Hg. Cardiac index decreased during VT (2.2 +/- 0.5 to 1.8 +/- 0.5 liters/min/m2 p less than 0.05), but in each case improved by the addition of atrial pacing, to 1.9 +/- 0.5 liters/min/m2. Evidence from pressure recordings suggested that optimal atrial pacing resulted in atrial contraction in early left ventricular diastole. Thus, appropriately timed atrial pacing during VT can result in significant increases in blood pressure and a consistent increase in cardiac index. In addition to offering insight into the mechanisms of hemodynamic compromise during VT, the clinical use of this technique may be to improve hemodynamic values in patients with hemodynamically unstable VT.